Similar Datasets
Project description:Azorhizobium doebereinerae overview
| PRJNA163199 | ENA
Project description:Salmonella Heidelberg is currently the 9th common serovar and has more than twice the average incidence of blood infections in Salmonella. A recent Salmonella Heidelberg outbreak in chicken infected 634 people during 2013-2014, with a hospitalization rate of 38% and an invasive illness rate of 15%. While the company’s history suggested longstanding sanitation issues, the strains’ characteristics which may have contributed to the outbreak are unknown. We hypothesized that the outbreak strains of S. Heidelberg might possess enhanced stress tolerance or virulence capabilities. Consequently, we obtained nine food isolates collected during the outbreak investigation and several reference isolates and tested their tolerance to processing stresses, their ability to form biofilms, and their invasiveness in vitro. We further performed RNA-sequencing on three isolates with varying heat tolerance to determine the mechanism behind our isolates’ enhanced heat tolerance. Ultimately, we determined that (i) many Salmonella Heidelberg isolates associated with a foodborne outbreak have enhanced heat resistance (ii) Salmonella Heidelberg outbreak isolates have enhanced biofilm-forming ability under stressful conditions, compared to the reference strain (iii) exposure to heat stress may also increase Salmonella Heidelberg isolates’ antibiotic resistance and virulence capabilities and (iv) Salmonella Heidelberg outbreak-associated isolates are primed to better survive stress and cause illness. This data helps explain the severity and scope of the outbreak these isolates are associated with and can be used to inform regulatory decisions on Salmonella in poultry and to develop assays to screen isolates for stress tolerance and likelihood of causing severe illness.
2018-09-01 | GSE103418 | GEO
Project description:Azorhizobium nodulans AA-N062 genome sequencing
| PRJNA346208 | ENA
Project description:A food-borne outbreak of haemorrhagic colitis (HC) and HUS caused by E. coli O103:H25 occurred in Norway, 2006. The outbreak included 17 registered cases, of which 10 developed HUS. The aim of this study was to characterize two E. coli O103:H25 isolates from this outbreak. Only one of the isolates carry the stx2 gene (by PCR). Since they have the same typing profile by typing method MLVA, we expect the isolates to have identical gene content except from an Stx2-encoding phage. Therefore, we further investigate whether the Stx2-encoding phage has any impact on the gene expression. Keywords: mixed, gene expression, comparative genomic hybridization Triplicate samples of mRNA from a test strain O157:H7 EDL933 and two outbreak strains - one Stx positive and one stx negative were co-hybridized with genomic DNA from the same strain. Triplicate samples of the Stx positive strain grown at acidic conditions was also co-hybridized with genomic DNA from the Stx positive strain. Genomic DNA for each strain is technical replicates only.
2010-09-01 | E-GEOD-9418 | biostudies-arrayexpress
Project description:Azorhizobium sp. AG788 Genome sequencing and assembly
| PRJNA463037 | ENA
Project description:A food-borne outbreak of haemorrhagic colitis (HC) and HUS caused by E. coli O103:H25 occurred in Norway, 2006. The outbreak included 17 registered cases, of which 10 developed HUS. The aim of this study was to characterize two E. coli O103:H25 isolates from this outbreak. Only one of the isolates carry the stx2 gene (by PCR). Since they have the same typing profile by typing method MLVA, we expect the isolates to have identical gene content except from an Stx2-encoding phage. Therefore, we further investigate whether the Stx2-encoding phage has any impact on the gene expression. Keywords: mixed, gene expression, comparative genomic hybridization
2010-09-01 | GSE9418 | GEO
Project description:An array analysis of C. gattii (C. bacillosporus), intended to identify loci associated with the hypervirulence of the Vancouver Island Outbreak (VIO). 23 C. gattii isolates, representing both VIO strains and control strains, were grown for 24 hours in mammalian macrophages. RNA was isolated and gene expression for each strain quantified relative to pooled RNA from all 23 samples. Linear regression was used to identify loci showing positive or negative correlation with "intracellular proliferation rate", a proxy measure for virulence. Data from this analysis is included in Ma et al, 2009, PNAS 106(31) 12980-12985. The abstract is included below. In 1999, the population of Vancouver Island, Canada, began to experience an outbreak of a fatal fungal disease caused by a highly virulent lineage of Cryptococcus gattii. This organism has recently spread to the Canadian mainland and Pacific Northwest, but the molecular cause of the outbreak remains unknown. Here we show that the Vancouver Island outbreak (VIO) isolates have dramatically increased their ability to replicate within macrophages of the mammalian immune system in comparison with other C. gattii strains. We further demonstrate that such enhanced intracellular parasitism is directly linked to virulence in a murine model of cryptococcosis, suggesting that this phenotype may be the cause of the outbreak. Finally, microarray studies on 24 C. gattii strains reveals that the hypervirulence of the VIO isolates is characterized by the up-regulation of a large group of genes, many of which are encoded by mitochondrial genome or associated with mitochondrial activities. This expression profile correlates with an unusual mitochondrial morphology exhibited by the VIO strains after phagocytosis. Our data thus demonstrate that the intracellular parasitism of macrophages is a key driver of a human disease outbreak, a finding that has significant implications for a wide range of other human pathogens. Dual-colour hybridization (each sample was hybridized against pooled RNA), one array per isolate, 23 biological samples, no technical replicates.
2010-05-15 | E-GEOD-17052 | biostudies-arrayexpress
Project description:An array analysis of C. gattii (C. bacillosporus), intended to identify loci associated with the hypervirulence of the Vancouver Island Outbreak (VIO). 23 C. gattii isolates, representing both VIO strains and control strains, were grown for 24 hours in mammalian macrophages. RNA was isolated and gene expression for each strain quantified relative to pooled RNA from all 23 samples. Linear regression was used to identify loci showing positive or negative correlation with "intracellular proliferation rate", a proxy measure for virulence. Data from this analysis is included in Ma et al, 2009, PNAS 106(31) 12980-12985. The abstract is included below. In 1999, the population of Vancouver Island, Canada, began to experience an outbreak of a fatal fungal disease caused by a highly virulent lineage of Cryptococcus gattii. This organism has recently spread to the Canadian mainland and Pacific Northwest, but the molecular cause of the outbreak remains unknown. Here we show that the Vancouver Island outbreak (VIO) isolates have dramatically increased their ability to replicate within macrophages of the mammalian immune system in comparison with other C. gattii strains. We further demonstrate that such enhanced intracellular parasitism is directly linked to virulence in a murine model of cryptococcosis, suggesting that this phenotype may be the cause of the outbreak. Finally, microarray studies on 24 C. gattii strains reveals that the hypervirulence of the VIO isolates is characterized by the up-regulation of a large group of genes, many of which are encoded by mitochondrial genome or associated with mitochondrial activities. This expression profile correlates with an unusual mitochondrial morphology exhibited by the VIO strains after phagocytosis. Our data thus demonstrate that the intracellular parasitism of macrophages is a key driver of a human disease outbreak, a finding that has significant implications for a wide range of other human pathogens.
2009-08-07 | GSE17052 | GEO